The lab's research
objective is to improve
diagnosis and treatment
of chronic pain by
expanding our
understanding of its
neurochemistry and
neuropathology.

ANALGESIC PHARMACOLOGY

Many analgesic drugs, including
opioids like morphine, interact in a
synergistic manner when
co-administered. This is important
clinically as co-administration of
synergistic drug combinations can
maximize pain relief while
minimizing adverse side effects. We
investigate the molecular mechanism
underlying these interactions. This
information could help to design
safer, better tolerated and more
effective pharmacological treatments
for chronic pain.

PAIN EPIGENETICS

Epigenetics is a broad term used to
refer to chemical modifications to
DNA that regulate gene expression
such as DNA methylation, which is
linked to many diseases including
cancer and type II diabetes. In
collaboration with Dr. Moshe Szyf,
we are studying the epigenetic
regulation of chronic pain, which is
currently virtually unexplored. Our
demonstrated a role for epigenetic
regulation in chronic low back pain
in both mice and in humans (Tajerian
et al., 2011) was the
first demonstration of epigenetic
control of a single gene being
associated with a human chronic pain
condition. We recently received a
Neuropathic Pain Research Award from
Pfizer Canada to study the role of
DNA methylation in chronic pain in
the brain.

CHRONIC BACK PAIN

Persistent back pain is the most
common chronic pain condition in
Canadians age 65 and under. The vast
majority of individuals suffer for
years with little relief. This is
due, in part, to a lack of
understanding of the underlying
causes of back pain. We are engaged
in both pre-clinical and human
studies designed to understand the
pathophysiology of low back pain and
how it can be treated.

Pre-clinical Studies

Degeneration of the intervertebral
discs in the spine is associated
with increased risk of chronic low
back pain. Unfortunately, the
relationship between disc
degeneration and chronic pain is not
well understood. We have developed a
rodent model of back pain due to
degeneration of the spine as a tool
to study this phenomenon (Millecamps
et al., 2011, 2012). This model will
increase our understanding of the
relationship between disc
degeneration and pain and will allow
for the identification and testing
of novel therapeutic interventions
for the alleviation of chronic low
back pain.

Human Studies

Relationship between Intervertebral
Disc Degeneration, Innervation and
Low Back Pain:
Increases in nerve fibers within
degenerating discs has been proposed
as a mechanism contributing to
chronic pain. We are performing
anatomical and biochemical studies
on human lumbar discs obtained
surgically from chronic pain
patients and post-mortem from
transplant donors to understand the
relationship between low back pain,
disc degeneration and disc
innervation in humans.

Effect of treatment of chronic low
back pain on abnormal brain anatomy
and function:Chronic
pain is associated with pathological
changes in certain regions of the
brain. The consequences of these
changes are not yet fully
understood. We are using magnetic
resonance imaging in chronic low
back pain patients to address this
question. Our data indicates that
some pain-related changes in the
brain can be reversed by effective
treatment, suggesting that the brain
can recover from chronic pain. Our
first study on this topic (Seminowicz
et. al.) was published in the
Journal of Neuroscience
and received international coverage
in the lay press.

Human Biomarkers for Low Back Pain:A
biological marker or biomarker is
any characteristic that can be
measured and evaluated as an
indicator of normal biologic
processes, pathologic processes or
responses to therapeutic
intervention. We are currently
examining samples of cerebral spinal
fluid and saliva from patients with
chronic low back pain for potential
biomarkers using traditional
biochemical and cutting edge
proteomics methods (i.e. LC-MS/MS).
The identification of biomarkers for
chronic low back pain will provide
insight into its diagnosis and
treatment.